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LOCAL ANESTHETIC AGENTS

LOCAL ANESTHETIC AGENTS. History of local anesthesia. 1500’s Accounts referring to Peruvian Indians chewing on leaves of the coco plant are found

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LOCAL ANESTHETIC AGENTS

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  1. LOCAL ANESTHETIC AGENTS

  2. History of local anesthesia • 1500’s Accounts referring to Peruvian Indians chewing on leaves of the coco plant are found • 1884 Cark Koller demonstrated the usefulness of the extract from these leaves[cocaine]as atopical anesthetic for the eyes, and earned distinction as the “father of local anesthesia • 1884 Willium Halsted used cocaine in the first nerve block [ Inferior alveolar nerve block]. The use of cocaine for anesthesia produced several unwanted side effects including cardiac problem and addiction • 1885 James Corning demonstrated the use of a tourniquet to slow absorption of cocaine

  3. History of local anesthesia • 1901 Heinrich Braun demonstrated the use of epinephrine to retard local anesthetic absorption from the site of injection • 1904 Alfred Einhorn introduced procaine . Epinephrine was needed to constrict the vessels in the area of administration to lengthen the duration of anesthesia. It was common to see a 1:50,000 concentration for many years • 1943 Nils Lofgren introduced lidocaine • 1947 Novocol company made the dental aspirating syringe available • 1959 Disposable sterile needles made available by Cook- Waite, Roehr Company

  4. Physiology of nerve conduction

  5. Sodium-potassium Pump

  6. Channel Entry

  7. Local anesthetics:amides vs. esters

  8. Classification of local anesthetics

  9. Absorption • Site of injection • The dose of local anesthetic • Physicochemical properties of local anesthetic • The addition of epinephrine

  10. Distribution Systemic absorption heart brain Skeletal muscle Site of injection

  11. Biotransformation and Elimination Aminoester Aminoamide Plasma esterase Hepatic enzyme Renal excretion

  12. สภาพของผู้ป่วยกับการขับถ่ายยาสภาพของผู้ป่วยกับการขับถ่ายยา • อายุ – ผู้ป่วยสูงอายุขับถ่ายยาได้ช้าลง • โรคตับ – ทำให้ half life ของยานานขึ้น • cardiac output –ถ้ามี cardiac output ต่ำ จะขับถ่ายยาได้ช้าลง

  13. Potency: lipid solubility • Onset : pKa, concentration of local anesthetic

  14. What is pKa? pKa = pH + log[ RNH+ ] [RN] (modified Henderson- Hasselbalch equation) pKaisthe dissociation constant, represents the pH at which the concentration of the ionized base(RNH+) and the non-ionized base (RN) are equal.

  15. RNH+ RN + H+ Outside membrane Inside membrane • RNH+ RN + H+

  16. Exampleat physiologic pH (7.4) if lidocaine (pKa 7.9) is administered into an area of infection (pH 4.9) resulting 1,000:1 ionized to non-ionized indicates a poorer penetration into the nerve tissue and therefore a less effective nerve block

  17. Quinn and Malamed (1990) and Haegerstam(1990) suggested of administer L.A. AWAY from the area of inflammation (nerve block) especially in the area of EXTENSIVE CELLULITIS Malamed. Handbook of LOCAL ANESTHESIA 1990. Haegerstam, Introduction to Dental Local anesthesia 1990.

  18. Duration of action • Differential sensory/ motor blockade • Adverse reaction

  19. Clinical use of local anesthesia • Topical anesthesia • Infiltration • Peripheral nerve block • Epidural block • Spinal block • Intravenous regional anesthesia

  20. Toxicity

  21. Clinical sign and symptom LA toxicity

  22. CNS toxicity Potency The rate of intravenus administration Acid base status and PaCO2

  23. Cardiovascular toxicity

  24. CC/CNS Ratio • i.e. the ratio of the LA dosage required for irreversible cardiovascular collapse and the dosage that produces CNS toxicity (convulsions) • the higher the CC/CNS ratio the better the safety margin

  25. Prevention • Aspiration before injection • Inject slowly • Use smallest quantity of solution and lowest concentration of vasoconstrictor • Observe the patient after injection • Choose another anesthetic if the patient has tendency for allergic reaction

  26. The signs and symptoms of allergic reaction include: • generalized body rash or skin redness • itching, urticaria (hives) • bronchospasm (difficulty breathing) • swelling of the throat • asthma • abdominal cramping • irregular heartbeat • hypotension (low blood pressure) • swelling of the face and lips (angioneurotic edema)

  27. Adverse reactions of commonly usedlocal anesthetics • Methemoglobinemia associated with prilocaine, articaine, benzocaine • Local tissue toxicity

  28. epinephrine

  29. ReceptorResponse Alpha stimulation Vasoconstriction Peripheral resistance Beta 1 stimulation Heart rate Force of cardiac contraction Cardiac output Beta 2 stimulation Vasodilatation Bronchodilation Coronary blood flow

  30. Signs Elevated BP, HR Symptoms Fear Anxiety Restlessness Throbbing headache Tremor Dizziness Pallor Respiratory difficulty Palpitations Adverse reactions of vasopressor drugs

  31. Contraindication for Epinephrine • Blood pressure over 200 torr systolic or 115 torr diastolic • Uncontrolled hypertension • Severe cardiovascular disease including less than 6 months after a myocardial infarction or cerebrovascular accident • Daily episodes of angina pectoris or unstable angina • Cardiac dysrhythmias despite appropriate therapy • Medicated with beta blocker,monoamine oxidase inhibitor , or tricyclic antidepressant; or general anesthesia with a halogenated anesthetic like halothane

  32. New York Heart Association : แนะนำว่าควรใช้ epinephrine ในขนาด 3 ug. / kg. Body weight แต่ไม่ควรเกิน 0.2 mg. (200 µg) หากผู้ป่วยมีปัญหาเกี่ยวกับ โรคความดันโลหิตสูง โรคหัวใจ ให้ใช้ Epinephrine ในขนาด 40 ug และสูงสุด ไม่ควรเกิน 54 µgต่อการฉีดยาครั้งหนึ่ง

  33. วิธีคำนวณปริมาณของ Epinephrine • Epinephrine ขนาด 1 : 200,000 • 1 gm / 200,000 ml • 1,000 mg / 200,000 ml • 1 mg / 200 ml • 0.005 mg / 1 ml

  34. ผู้ป่วยเด็กอายุ 2 ปี หนัก 12 กิโลกรัม หกล้มมีแผลฉีกขาดที่นิ้ว ต้องเย็บแผล ควรใช้ยาชาชนิดใด ปริมาณและความเข้มข้นเท่าไร

  35. ผู้ป่วยชายอายุ 25 ปี น้ำหนัก 60 กิโลกรัม ไม่มีโรคประจำตัว บอกวิธีการให้ยาชาและปริมาณยาที่ใช้กับผู้ป่วย

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